Glial interfaces in neuroinflammation and neurodegeneration: Mechanisms to therapies

Glial cells have emerged as central regulators of neural homeostasis, immune surveillance, and disease propagation throughout the central nervous system (CNS)—including the brain, spinal cord, and retina. Their dynamic interactions with neurons and components of the neurovascular unit play a pivotal role in maintaining brain homeostasis and determining the outcome of neuroinflammatory responses. Increasing evidence highlights that their interactions with neurons and the neurovascular unit are fundamental in shaping the onset and progression of neurodegenerative diseases such as Alzheimer’s disease. Disruptions in glial communication and signaling at the neurovascular interface lead to impaired blood-brain barrier integrity, persistent inflammation, and neuronal dysfunction, thereby accelerating neurodegeneration.
This Research Topic aims to investigate the mechanisms by which glial cells influence neuroinflammation and neurodegeneration, focusing on their interactions with neurons, vascular cells, and peripheral immune components. Particular emphasis will be placed on understanding how astrocytes, microglia, and oligodendrocytes coordinate or miscommunicate within the neurovascular environment to modulate disease pathways. Studies addressing the molecular, metabolic, and signaling mechanisms that regulate glial function and their impact on neuronal survival and vascular health are of special interest.
Research exploring glial contributions to Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, glaucoma, and other age-related neurodegenerative conditions are especially encouraged. The collection welcomes experimental and translational studies that bridge basic mechanistic understanding with therapeutic innovation, including efforts to identify novel molecular targets, develop glia-focused interventions, and restore neurovascular communication.
Scope includes but not limited to:
• Microglial crosstalk and glial diversity: Cellular and molecular programs governing glial–glial and glial–neuronal interactions in neuroinflammation, synaptic remodeling, and degeneration.
• Glial dysfunction and aging-primed responses: Mitochondrial stress, autophagy failure, complement activation, and immune–glia signaling in the CNS and retina, including the effects of aging and systemic inflammation on glial sensitivity.
• Neurovascular and CNS–retina cross-system insights: Shared signaling mechanisms linking the neurovascular unit, blood–brain and blood–retina barriers, and glial homeostasis.
• Computational and systems neuroscience approaches: Network-based models, spatial transcriptomics, multi-omic integration, and AI-driven frameworks to map glial states and predict therapeutic outcomes.
• Therapeutic innovations: Glial- and vascular-targeted therapies, including gene editing, mitochondrial rescue, neurotrophic support, and anti-inflammatory or barrier-stabilizing strategies.

Article types and fees

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

• Brief Research Report
• Classification
• Clinical Trial
• Data Report
• Editorial
• FAIR² Data
• General Commentary
• Hypothesis and Theory
• Methods
• ... View all formats

Articles that are accepted for publication by our external editors following rigorous peer review incur a publishing fee charged to Authors, institutions, or funders.

Article types

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

• Brief Research Report
• Classification
• Clinical Trial
• Data Report
• Editorial
• FAIR² Data
• General Commentary
• Hypothesis and Theory
• Methods
• Mini Review
• Opinion
• Original Research
• Perspective
• Policy and Practice Reviews
• Review
• Study Protocol
• Systematic Review
• Technology and Code

Keywords: Glial cells, Neuroinflammation, Neurodegeneration, Glia-neuron interactions, Therapeutic strategies

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.